Duchenne's Muscular Dystrophy (DMD) is an X-linked genetic disease affecting 1 of 3500 boys born world-wide. The disease is clinically apparent between ages 2 and 3 years;a time coincident with increased load bearing muscle activity which is characterized by increases in metabolic and mechanical stress in the muscle. Given this fact, there is much interest in defining stress dependent pathways which contribute the pathogenic progression of the disease. Within the framework of the Human Response Model (M. M. Heitkemper &Shaver, 1989), I propose to focus on the biological response axis of DMD to further define cellular mechanisms which may contribute to stress dependent muscle damage. Within the muscle cell, two signaling pathways (i.e., calcium (Ca2+) signaling and reactive oxygen species (ROS)), have been implicated as factors which increase the pathogenic progression of the dystrophic process. However, these pathways have not been fully explored in the context of their stress dependent modulation. My preliminary data on each pathway in control, non-diseased muscle, demonstrate that these signaling pathways are enhanced during either mechanical or voltage stress. In this proposal I test my overall hypothesis that dystrophic muscle will have a further enhancement in the stress dependent signaling;a result which would be consistent with increased muscle damage due to aberrant Ca2+ or ROS signaling. As cure for this genetic disease is perhaps decades away, these finding may provide new insights into the role of muscle movement and activity dependent stress on the pathogenic progression of the dystrophic process;important information for nurses who are acutely interested in environmental or behavioral stimuli which may contribute to disease processes (M. M. Heitkemper &Shaver, 1989).